Abstract 14474: The Levels of Serum Insulin-Like Growth Factor Binding Protein (IGFALS) Decline Seven Days After Non-Emergent Cardiac Surgery - A Potential Link to Neuroinflammation?

Abstract

Introduction: Inflammatory response and metabolic derangements may accelerate neurodegeneration after cardiac surgery. Insulin, insulin growth factor (IGF), and insulin-like growth factor binding protein acid labile subunit (IGFALS) are the centerpieces of glucose metabolism, the critical factor determining long-term recovery from cardiac surgery and neurodegeneration progression[1]. IGFALS is a regulatory element of IGF that increases their half-life and vascular localization Hypothesis: We investigate the dynamics of IGFALS up to 3 months after cardiac surgery. We hypothesize that post-cardiac surgery IGFALS serum level abnormalities are related to changes in neuroinflammatory (BDNF, CXCL13) and neurodegeneration marker (tau). Methods: Patients (n=25) scheduled for non-emergent heart surgery were included, except for patients with pre-existing immunological aberrancies. Blood was collected before surgery(t baseline ), 24 hours later(t 24h ) after the first sample, 7 days(t 7d ), and 3 months(t 3m ) after t baseline . Variables regarding the surgery were collected from medical records. IGFALS levels were measured via ELISA, while neurodegeneration and neuroinflammation markers via multiplex technology. Results: Demographic variables had limited effects on IGFALS. The serum levels of IGFALS varied significantly (H[4;221]=9.146; 0.0274) (Figure 1). The serum levels were significantly lower at t 7d but recovered at t 3m . During the acute inflammatory response at t 24h IGFALS, serum levels remained unaltered. BDNF at 3m correlated with IGFALS at t 7d ( r 2 =0.38;p=0.012) and t 3m ( r 2 =0.39;p=0.018). CXCL13 demonstrated similar interactions. Tau level did not correlate with IGFALS dynamics. Conclusions: The data demonstrated a significant long-term decline in IGFALS level after cardiac surgery. The correlations suggest a potential link between IGFALS and some neuroinflammatory markers. 1. Westwood, A.J Neurology, 2014.82(18): p. 1613-9.